Sodium (Na+) is an essential nutrient, but humans consume this nutrient in excess which increases the risk of hypertension and stroke. It is currently unknown which cell type within taste buds is responsible for Na+-taste transduction. Here, an optogenetic approach is used to determine whether Type I cells within taste buds are responsible for Na+ taste transduced through epithelial sodium channels (ENaCs). Optogenetic manipulation of Type I taste-bud cells allows for selective perturbation of taste-bud circuity with an unprecedented level of precision? unmatched by conventional pharmacology?and serves as a valuable tool for unraveling the enigma of the taste of Na+. This project will test two hypotheses. 1) Optogenetic activation (via Channelrhodopsin-2; ChR2) of Type I cells in fungiform-taste buds activates NaCl-best neurons in the mouse Nucleus Tractus Solitarius (NTS), located in the medulla. 2) Optogenetic activation (via ChR2) of Type I cells in fungiform taste buds elicits Na+ taste and drives Na+ appetite in Na+ deprived mice. Knowledge obtained from these investigations will provide the field with much needed information about the role of Type I cells in taste function, and could provide a target for pharmacological manipulation of taste circuitry to enhance salt taste, thereby decreasing Na+ intake. Such discoveries would have a positive impact on human health and disease afflicted by excess Na+ consumption.